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Cell Mol Neurobiol. 2015 May;35(4):483-91. doi: 10.1007/s10571-014-0142-x. Epub 2014 Nov 22.

Administration of antagomir-223 inhibits apoptosis, promotes angiogenesis and functional recovery in rats with spinal cord injury.

Author information

1
Department of Orthopaedic Surgery, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, People's Republic of China, daliumail@163.com.

Abstract

MicroRNAs (miRNAs) are recently described as a class of short non-coding RNAs, which play important roles in post-transcriptional gene regulation and involved in many physiological and pathological processes. MicroRNA-223 (miR-223) has been showed highly elevated in the injured spinal cord. However, the potential role and underlying mechanisms of miR-223 in spinal cord injury (SCI) were incompletely understood. In the present study, we observed the persistent high levels of miR-223 in the injured spinal cord at different time points (1, 3, 7, and 14 days) after SCI. Besides, inhibiting miR-223 by intrathecally injection with antagomir-223 significantly improved recovery in hindlimb motor function and attenuated cell apoptosis in spinal cord-injured rats. Additionally, antagomir-223 treatment markedly decreased the pro-apoptotic protein levels, including Bax and cleaved caspase-3, up-regulated the anti-apoptotic Bcl-2 protein level, as well as the expression of GluR2. Moreover, inhibition of miR-223 promoted angiogenesis, as evidenced by the increased CD31 expression and microvascular density. Taken together, our results indicate that inhibition of miR-223 with antagomir-223 exerts protective role in functional recovery, angiogenesis, and anti-apoptosis during SCI. Thereby, miR-223 may be a promising target of therapy for SCI.

PMID:
25416533
DOI:
10.1007/s10571-014-0142-x
[Indexed for MEDLINE]

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